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1 number 14 Done by Deena nafea Corrected by Ensherah Mokhemar Doctor Hamed Al-Zoubi
2 - In this sheet we are going to talk about 4 types of bacteria : PSEUDOMONAS BRUCELLA LEGIONELLA CAMPYLOBACTER HELICOBACTER PYLORI (H. PYLORI) Pseudomonas - Pseudomonas is a family, while the subtypes are listed below: Pseudomonas aeruginosa Burkholderia pseudomallei Burkholderia cepacia 1-Most of them are saprophytes, they are widely distributed in aquatic environments (sinks, hospitals) *Saprophytes: microorganisms that live on dead or decaying organic matter. 2- They are multi drug resistant (especially, the hospital acquired) 3- They are a major cause of nosocomial infections (Hospital-acquired infections). 4- They are oxidase positive aerobic gram-negative rods 5- They are motile, having 1-2 flagella. 6- They produce pigments, pigmented colonies with cut grass or grape like smell. blue pigment, pyocyanin, and the yellow green fluorescent pigment pyoverdin This bacterium gives colonies, infected wounds and the burned skin dressings with pigments. Virulence factors - Pigment production
3 -Exotoxin A EF2 (elongation factor 2) -Protease -Polysaccharide - Secretion of Exopolysaccharide (Alginate like) which is responsible for the mucoid colonial phenotype (this makes the bacteria resistant to the antibiotic) Infections Community and hospital acquired - Community acquired infections: otitis externa (external ear canal infection) and renal failure -Hospital acquired infections (nosocomial infections); they are serious and have a high mortality rate because they are multi drug resistant. -Inherited Cystic fibrosis and lung diseases - Chronic obstructive pulmonary disease (COPD) Diagnosis -Selective media containing acetamide -Commercial kits -PCR (polymerase chain reaction) Treatment Follow lab sensitivity test Brucella (Malta fever) Brucellae are highly infectious gram-negative coccobacilli that cause a septicaemic illness, undulant fever. (it could be fatal)
4 Undulant fever is characterised by being wavy, interchangeable between high and low fever, it is caused by TB, BRUCELLA and salmonella. Most human diseases are caused by Brucella melitensis, B. abortus or B. suis B.melitensis in sheep and goats B.abortus in kittens B.suis in pigs Typical zoonosis is most commonly acquired from infected animals, or from infected meat or dairy products. Non-motile LPS Killed at a temperature of 60 C for 10 min Sensitive to direct sunlight and moderately sensitive to acid Infection: Incubation period is usually about days The organisms are intracellular parasites and subsequently localize in various parts of the reticuloendothelial system with the formation of abscesses or granulomatous lesions, resulting in complications that may involve any part of the body reticuloendothelial system: spleen, bone marrow, liver, lymph nodes. Brucellosis can present as an acute or subacute pyrexial illness that may persist for months or develop into a focal infection that can involve almost any organ system (undulant fever\ osteomyelitis \abscess in the back, liver, bone) Diagnosis
5 Firstly, ask the patient if he drinks milk or any dairy products then proceed with laboratory tests. Brucella sample must be treated as high risk; it could be transmitted by inhalation and it could be transmitted to the lab. 1- Repeated blood culture (I. Cellular organism ), B.M. Take the blood sample 3-4 times, take it from bone marrow, spleen. Incubated for 6-8 weeks 2- Serology (more effective diagnosis than culture) Detect lipopolysaccharide antigens Serologic tests are blood tests that look for antibodies in your blood. 3. PCR Treatment Streptomycin or gentamicin with tetracycline Co-trimoxazole and rifampicin can be used in children and pregnant women Legionella pneumophila Weak gram-negative bacilli Silver stain is used, but not gram stain because it is very hard to see it using gram stain Virulence factors: LPS, penicillinase, cytotoxins and haemolysins Incubation: 2-10 days Transmitted through Water droplets from Air conditions, towers... But it can't be transmitted from person to person Outcome infections:
6 Pneumonia known as legionnaires disease which is severe is accompanied by sputum and fever with hyponatremia (low sodium concentration, lower than 130) Less serious influenza-like illness called Pontiac fever Diagnosis It needs special media, buffered charcoal yeast extract agar (BCYE), which contains iron plus cysteine as an essential growth factor (colonies have cut glass appearance under microscope) - l. pneumophila could be diagnosed through urine to detect the presence of antigen in the sample, because lipopolysaccharide is excreted in a high concentration in the urine Treatment: Macrolides such as: azithromycin and clarithromycin - Remember: it is resistant to penicillin Control: No vaccine but chlorinating and heating water Campylobacter The main human pathogen is campylobacter jejuni (C. jejuni) Habitat: Guts of various animal species such as chickens, domestic animals and seagulls Remember: Brucella and campylobacter are zoonotic infections Pathogenesis: Enterocolitis (GI INFECTION) may penetrate beyond the mucosa Small gram negative, curved or spiral rods (Figure/seagull appearance). Highly motile (darting, corkscrew like movement), with a flagellum at one or both ends
7 Microaerophilic (5% O2, 10-15% CO2, 80% Nitrogen) Grow at 42 C for 2 days (25 C no growth, 37 C some growth, 42 C enhanced growth). Needs a special media (Skirrow s) Clinically: Incubation period: 1-10 days Route of transmission: Eating contaminated poultry, other meat or drinking milk, Faecal oral route between humans can occur Bloody diarrhoea with mucus (up to 20 stools a day > faecal incontinence) Abdominal pain is a prominent feature (mimicking appendicitis) Septicaemia with fever and rigors in severe cases Symptoms may last several days, and relapses are common (usually self limiting) Guillain-Barre syndrome as a complication, like influenza virus. It happens after campylobacter, in which autoimmune antibodies attack myelin sheath causing a demyelination from the neuron, causing paralysis data to be sent from down to the above reaching the respiratory muscles, which could be fatal. Caution: Aspirin is contraindicated to a child with mild fever Diagnosis Stool sample for culture on Skirrow s medium Treatment: Erythromycin in severe cases. Ciprofloxacin as an alternative but resistance is increasing
8 Helicobacter pylori (spiral bacteria associated with peptic ulcer) In 1985, the scientist Marshall persuaded people that H. pylori was responsible for stomach ulcers, but they were not convinced, because the stomach was an acidic environment and it kills the bacteria. The scientist wanted to prove to them that he was right, he asked them to take a stomach biopsy from him which would show them that there was no ulcer in his duodenum. Then he drank the culture (H. pylori) and asked for another biopsy after 8 days, the result was he had an ulcer. Thus, it was found that the bacteria did not die but multiplied and then convinced the others that H.pylori causes ulceration. Most of us get infected by this bacteria at childhood, which causes gastritis. Properties Gram negative, spiral, flagellated (motile) bacilli H. pylori tuft of 4-6 sheathed flagella attached at one- pole. Slow growing, require complex media, microaerophilic (require carbon dioxide, some Oxygen and Nitrogen) Oxidase, catalase and Urease positive - Urease: converts urea to carbon dioxide and ammonia Ammonia (which is base) surrounds the bacteria to protect it from the acidic secretion of the stomach. Proliferates in mucus overlying gastric antral mucosa > non-invasive. Culture: On special medium containing vancomycin, polymyxin and trimethoprim (Skirrow s) At 37 C for 3-7 days in microaerophilic conditions. Epidemiology:
9 Man (Not zoonatic) appears to be the sole reservoir and source of H. pylori. How infection is transmitted is unknown, but it is presumed to be by the oral-oral or, possibly, faecal-oral route. Infection rates are strongly related to poor living conditions and overcrowding during childhood. Nosocomial infection from inadequately disinfected endoscopes has also occurred Remarkably, H. pylori, colonizes roughly half of the world's Population It is symptomatic in some people and asymptomatic in others. Pathogenesis Sheathed flagella lophotrichous motile Enables penetration into viscous environment (mucus) Adhesions: Heme agglutinins; Sialic acid binding-adhesion Mucinase: Degrades gastric mucus to be able to move and affords a basic environment to live in; Localized tissue- damage Urease converts urea (abundant in saliva and gastric juices) into bicarbonate (to CO2) and ammonia Neutralize the local acid environment Localized tissue damage Vacuolating toxin (VacA) and cytotoxins (CagA) Epithelial cell damage The vacuolating toxin has been associated with pore- formation in host cell membranes, the loosening of the tight junctions between epithelial cells (thus affecting mucosal barrier permeability causing vacualation) Protection from phagocytosis & intracellular killing: Superoxide dismutase Catalase
10 Clinically: Symptomless Acute infection (when it transmitted for the first time during childhood): gastritis, severe Abdominal pain with fever lasting for 7-8 days, vomiting and fever may exist but no disseminated stage Chronic active gastritis; Type B. Gastric (70%) and duodenal ulcers (more than 90%). The symptoms of duodenal ulcer decrease when drinking cold milk or eating, and increases when the stomach becomes empty (opposite to gastric ulcers) Non-ulcer dyspepsia *dyspepsia : indigestion. Gastric malignancies. * gastric ulcers are more dangerous than peptic ulcer (more likely to become malignant) *Even in asymptomatic people you should treat them for H.pylori because the gastric ulcer could appear after years and become malignant. * There are other causes for gastric and peptic ulcers like: chemotherapy, burns. Diagnosis Definitive tests for H. pylori infection depend on finding the Organism in specimens of gastric mucosa obtained by biopsy. (In practice, non-invasive tests are used for initial screening not endoscopy). 1- Non-invasive tests: 1. Urea breath test 2. Faecal antigen 3. PCR 4. Serology
11 2. Invasive tests (endoscopy guided biopsies): To search for ulcers and tissue damage, if either one is found take a biopsy for histopathology, another one for culture (for maximum sensitivity 2 specimens are taken). Ideally, patients for endoscopy should not have received antibiotics or proton pump inhibitors for 1 month before the test. Treatment Life style change: Smoking, any food that irritates the stomach ulcers (different from one person to another)could be fats,yoghurt, coffee Triple therapies: Have reported cure rates from 85-90%. Administered for days. There is more than one regimen e.g.: Lansoprazole, amoxicillin, and clarithromycin * The doctor said that it is important to know that triple therapies are applied to H. pylori, without knowing their names)
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